Hypophosphatemia Follow-up

  • Author: Eleanor Lederer, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Feb 13, 2012
 

Further Inpatient Care

  • Follow-up phosphate determinations are helpful in establishing whether the patient has had a transient reversible episode of hypophosphatemia or a more chronic condition. Even in cases of established phosphate deficiency, most individuals respond readily to oral or parenteral phosphate repletion, and phosphate levels normalize within a few days. In contrast, phosphate wasting syndromes characteristically are refractory to vigorous supplementation.
  • If evidence of vitamin D deficiency is found, then the cause should be determined and corrected if possible.
    • Dietary education and vitamin D supplements should be provided.
    • If the patient has vitamin D deficiency due to drug-induced metabolism, discontinuation of the drug should be considered. However, in some circumstances, such as with the use of phenytoin, drug discontinuation may not be possible, and the patient should be instructed on the importance of daily vitamin D supplementation. To ensure that these patients maintain adequate vitamin D action, the 1,25 dihydroxy or active form of the vitamin can be administered.
    • Vitamin D deficiency may also suggest the possibility of significant intestinal malabsorption, which should be investigated.
  • Phosphate deficiency may also result from eating disorders. In appropriate clinical circumstances, this possibility should be explored with the patient and counseling should be provided if necessary. An inability to eat an adequate diet because of socioeconomic circumstances, dental inadequacies, or swallowing difficulties should be investigated and addressed.
  • Phosphate deficiency due to congenital wasting disorders often leads to severe osteomalacia. Bone films are warranted to determine and assess the severity of osteopenia. In some cases, bone biopsy might be helpful in determining optimal treatment.
  • Acquired phosphate wasting syndromes should prompt a search for the cause.
    • Hyperparathyroidism, if found, can be treated surgically or medically, depending on the clinical situation. Bone films and bone densitometry studies can help determine the severity of the bone loss that has occurred.
    • Proximal renal tubular disorders leading to hypophosphatemia are often accompanied by renal glycosuria, aminoaciduria, hypouricemia, and type II renal tubular acidosis due to bicarbonate wasting. These other manifestations of proximal tubule dysfunction are easily diagnosed, and the constellation of findings suggests heavy metal intoxication or paraproteinemia. Serum and urine protein electrophoresis and urinary metal screens are indicated for further evaluation.
    • When severe and accompanied by bone pain, phosphate wasting with hypophosphatemia in an adult should suggest the possibility of oncogenic osteomalacia. This paraneoplastic syndrome is caused by a circulating phosphate wasting factor secreted by certain tumors, especially tumors of mesenchymal origin.
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Further Outpatient Care

  • For transient hypophosphatemia, no further evaluation is required. In some clinical situations, periodic determination of serum phosphate concentration may be required, for example, in phenytoin-induced vitamin D deficiency.
  • If a patient undergoes parathyroidectomy for hyperparathyroidism, calcium and phosphate levels should be monitored postoperatively to assess the adequacy of the procedure and to ensure that the remaining parathyroid tissue is adequate to maintain mineral balance. In the vast majority of cases of primary hyperparathyroidism, calcium and phosphate levels normalize virtually immediately postoperatively and remain stable thereafter.
  • For phosphate wasting syndromes, periodic monitoring of bone density and bone films can help in assessing the degree of end organ damage.
  • For hypophosphatemia due to eating disorders, continued outpatient counseling and monitoring for signs of malnutrition are required.
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Inpatient & Outpatient Medications

  • Phosphate supplements are available in capsule or powder form. Because intestinal absorption of phosphate is typically excellent, phosphate supplements administered twice a day are generally adequate.
  • Vitamin D supplements in the form of ergocalciferol (D-2) or 1,25 dihydroxyvitamin D-3 are appropriate for patients with vitamin D deficiency. For patients with renal insufficiency, the active 1,25 form is more appropriate.
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Transfer

  • Although severe hypophosphatemia can be a medical emergency, parenteral phosphate is available in all hospital formularies and is the treatment of choice for severe hypophosphatemia. Therefore, transfer to another facility is rarely, if ever, needed.
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Deterrence/Prevention

  • Patients with hypophosphatemia due to eating disorders such as anorexia or bulimia require counseling and dietary therapy.
  • Patients with hypophosphatemia due to nonpsychiatric eating disorders, such as those elicited by poor socioeconomic status, dental problems, or swallowing difficulties, should receive dietary counseling and monitoring. The patients should be educated about the necessity for a balanced diet and should be encouraged to ingest full nutritional supplements. Continued dietary follow-up care can help prevent further relapses.
  • Patients who have recurrent hypophosphatemia should be discouraged from ingesting large quantities of antacids because they bind intestinal phosphate and block absorption.
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Complications

  • Complications of hypophosphatemia depend on severity and chronicity.
    • Mild transient hypophosphatemia yields no complications. Studies in patients with diabetic ketoacidosis undergoing intensive insulin therapy show that they often develop mild hypophosphatemia during the course of therapy. However, the hypophosphatemia produces no discernible problems, and treatment with supplemental phosphate has no effect on recovery.
    • Moderate hypophosphatemia can lead to muscle weakness.
      • This complication can be particularly important to recognize in the ICU, where hypophosphatemia can lead to respiratory muscle depression and impaired cardiac output.
      • Treatment of hypophosphatemia in this setting can increase cardiac output and facilitate weaning from the ventilator.
      • Moderate hypophosphatemia can also have consequences on renal function, specifically, mild metabolic acidosis and hypercalciuria.
  • The acute hypophosphatemic syndrome described in previous sections can have severe complications.
    • Although all of the organ effects are reversible with treatment, the clinical picture is dramatic and potentially fatal if not recognized.
    • These patients can have seizures, delirium, coma, or focal neurologic findings. They develop heart failure, rhabdomyolysis, acute hemolysis, leukocyte dysfunction, and abnormal results from liver function tests. Heart failure, rhabdomyolysis, and hemolysis can produce acute renal failure because of poor flow and pigment damage. Leukocyte dysfunction increases susceptibility to infection. These patients can also exhibit platelet dysfunction, glucose intolerance, and metabolic acidosis.
  • Chronic hypophosphatemia due to phosphate wasting produces a predominantly bone pathology. In children, the resulting rickets leads to short stature and significant bony deformities associated with abnormal bone mineralization. Adults develop osteomalacia with accompanying severe bone pain and fractures.
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Prognosis

  • The prognosis for a treatable and usually transient cause of hypophosphatemia is excellent. Discontinuation of antacids in cases of antacid abuse, ingestion of a normal diet in patients with eating disorders, or parathyroidectomy for patients with hyperparathyroidism are all examples of curable hypophosphatemia.
  • The prognosis for phosphate wasting syndromes is also largely dependent on the underlying cause. For hyperparathyroidism, parathyroidectomy is curative. For vitamin D deficiency (a combination of poor absorption and renal wasting), replacement of vitamin D is curative. On the other hand, X-linked hypophosphatemic rickets and vitamin – resistant rickets are only partially treatable with present medications and result in lifelong skeletal deformities.
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Patient Education

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Contributor Information and Disclosures
Author

Eleanor Lederer, MD  Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Coauthor(s)

Rosemary Ouseph, MD  Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Snehal Patel, MD  Fellow, Department of Nephrology, University of Louisville School of Medicine

Snehal Patel, MD is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Kentucky Medical Association, and Renal Physicians Association

Disclosure: Nothing to disclose.

Specialty Editor Board

James W Lohr, MD  Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Alexion Salary Employment

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA  Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

We wish to thank Deepak Mittal, MD, and Datinder Deo, MD, for their previous contributions to this article.

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